Our studies in FY 2008 focused on further analysis of the mode of action whereby copolymers inhibit development of experimental autoimmune uveitis (EAU). The copolymer we used was "YFAK", a novel molecule that was found in FY 2007 to inhibit EAU more efficiently than Copaxone (glatiramer acetate), a compound that is widely used for treatment of multiple sclerosis. The inhibitory effect of YFAK is demonstrated when the copolymer is administered in emulsion together with the uveitogenic antigen, IRBP. The inhibitory effect of YFAK could be attributed to two mechanisms: (a) the copolymer's capacity to compete with the uveitogenic antigen for the MHC molecules on the antigen presenting cells, or (b) the copolymer stimulates Th2 type suppressor cells, as suggested in our FY 2007 studies. We tested the former hypothetical explanation by administering YFAK in emulsion along with or separately from the uveitogenic antigen. We immunized groups of mice with emulsions containing the following: (i) IRBP, no YFAK; (ii) IRBP together with YFAK and (iii) IRBP separately from YFAK. EAU severity was the highest in group (i), minimally in group (ii) and intermediate in group (iii). [unreadable] [unreadable] These data thus support the notion that YFAK inhibits EAU development by the competition mechanism. It is assumed, however, that the copolymer also initiates development of suppressor Th2 cells, as demonstrated in our previous studies (FY 2007).